CHROMOSOME-11 ALLELE IMBALANCE AND CLINICOPATHOLOGICAL CORRELATES IN OVARIAN-TUMORS

被引:48
作者
GABRA, H
TAYLOR, L
COHEN, BB
LESSELS, A
ECCLES, DM
LEONARD, RCF
SMYTH, JF
STEEL, CM
机构
[1] WESTERN GEN HOSP,MRC,HUMAN GENET UNIT,EDINBURGH EH4 2XU,MIDLOTHIAN,SCOTLAND
[2] WESTERN GEN HOSP,DEPT PATHOL,EDINBURGH EH4 2XU,MIDLOTHIAN,SCOTLAND
[3] UNIV SOUTHAMPTON,CRC,GENET EPIDEMIOL UNIT,SOUTHAMPTON,HANTS,ENGLAND
[4] UNIV ST ANDREWS,SCH BIOL & MED SCI,ST ANDREWS,FIFE,SCOTLAND
关键词
CHROMOSOME; 11; TUMOR-SUPPRESSOR GENES; OVARIAN CANCER; LOSS OF HETEROZYGOSITY;
D O I
10.1038/bjc.1995.340
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Allele imbalance on chromosome 11 loci in ovarian cancer is a frequent event, suggesting the presence of tumour-suppressor genes for ovarian carcinogenesis on this chromosome. Ten highly polymorphic (CA) repeat microsatellites were used to determine allele imbalance in 60 primary ovarian rumours, including 47 epithelial ovarian cancers (EOCs). Forty EOCs (85%) showed allele imbalance at one or more loci, and in 39 of these (83%) the data suggested subchromosomal deletions: eight of lip only; six of 11q only; and 25 of both lip and 11q. Three consensus regions of deletion were indicated at 11p15.5-p15.3, 11q12-q22 and 11q23.3-q24.1. Allele imbalance at the 11q subtelomeric region (D11S912) correlated significantly with adverse survival, while imbalance at 11q14.3 and retention of heterozygosity al 11q22 (close to the site of the progesterone receptor gene) were associated with favourable clinicopathological features. The findings allow development of a preliminary model for the molecular evolution of epithelial ovarian cancer.
引用
收藏
页码:367 / 375
页数:9
相关论文
共 35 条
[1]   CLUES TO THE PATHOGENESIS OF FAMILIAL COLORECTAL-CANCER [J].
AALTONEN, LA ;
PELTOMAKI, P ;
LEACH, FS ;
SISTONEN, P ;
PYLKKANEN, L ;
MECKLIN, JP ;
JARVINEN, H ;
POWELL, SM ;
JEN, J ;
HAMILTON, SR ;
PETERSEN, GM ;
KINZLER, KW ;
VOGELSTEIN, B ;
DELACHAPELLE, A .
SCIENCE, 1993, 260 (5109) :812-816
[2]   CHROMOSOME-ABERRATIONS IN METASTATIC OVARIAN-CANCER - RELATIONSHIP WITH ABNORMALITIES IN PRIMARY TUMORS [J].
BELLO, MJ ;
REY, JA .
INTERNATIONAL JOURNAL OF CANCER, 1990, 45 (01) :50-54
[3]   ANALYSIS OF THE 11P13 WILMS-TUMOR SUPPRESSOR GENE (WT1) IN OVARIAN-TUMORS [J].
BRUENING, W ;
GROS, P ;
SATO, T ;
STANIMIR, J ;
NAKAMURA, Y ;
HOUSMAN, D ;
PELLETIER, J .
CANCER INVESTIGATION, 1993, 11 (04) :393-399
[4]   ISOLATION AND CHARACTERIZATION OF A ZINC FINGER POLYPEPTIDE GENE AT THE HUMAN CHROMOSOME-11 WILMS TUMOR LOCUS [J].
CALL, KM ;
GLASER, T ;
ITO, CY ;
BUCKLER, AJ ;
PELLETIER, J ;
HABER, DA ;
ROSE, EA ;
KRAL, A ;
YEGER, H ;
LEWIS, WH ;
JONES, C ;
HOUSMAN, DE .
CELL, 1990, 60 (03) :509-520
[5]   A COMPARISON OF PROCEDURES FOR ANALYZING MICROSATELLITE (CA)-REPEAT POLYMORPHISMS [J].
COHEN, BB ;
WALLACE, MR ;
CRICHTON, DN .
MOLECULAR AND CELLULAR PROBES, 1992, 6 (05) :439-442
[6]   ASSIGNMENT OF 112 MICROSATELLITE MARKERS TO 23 CHROMOSOME-11 SUBREGIONS DELINEATED BY SOMATIC HYBRIDS - COMPARISON WITH THE GENETIC-MAP [J].
COUILLIN, P ;
LEGUERN, E ;
VIGNAL, A ;
FIZAMES, C ;
RAVISE, N ;
DELPORTES, D ;
REGUIGNE, I ;
ROSIER, MF ;
JUNIEN, C ;
VANHEYNINGEN, V ;
WEISSENBACH, J .
GENOMICS, 1994, 21 (02) :379-387
[7]  
ECCLES DM, 1992, ONCOGENE, V7, P2069
[8]  
ECCLES DM, 1990, ONCOGENE, V5, P1599
[9]  
ECCLES DM, 1992, DIS MARKERS, V10, P95
[10]  
EHLEN T, 1990, ONCOGENE, V5, P219